BMC Molecular and Cell Biology最新文献

{"title":"CTC together with Shh and Nrf2 are prospective diagnostic markers for HNSCC.","authors":"Md Mizanur Rahman, Muhammad Mosaraf Hossain, Shafiqul Islam, Ridwan Ahmed, Mohit Majumder, Shantu Dey, Md Kawser, Bishu Sarkar, Md Ejajur Rahman Himu, Ali Asgar Chowdhury, Shakera Ahmed, Supran Biswas, Mostafa Mahfuzul Anwar, Mohammad Jamal Hussain, Rajib Kumar Shil, Sunanda Baidya, Ramendu Parial, Mohammed Moinul Islam, Atul Bharde, Sreeja Jayant, Gourishankar Aland, Jayant Khandare, Shaikh Bokhtear Uddin, Abu Shadat Mohammod Noman","doi":"10.1186/s12860-024-00500-0","DOIUrl":"10.1186/s12860-024-00500-0","url":null,"abstract":"<p><strong>Background: </strong>The lack of appropriate prognostic biomarkers remains a significant obstacle in the early detection of Head and Neck Squamous Cell Carcinoma (HNSCC), a cancer type with a high mortality rate. Despite considerable advancements in treatment, the success in diagnosing HNSCC at an early stage still needs to be improved. Nuclear factor erythroid 2-related factor 2 (Nrf2) and Sonic Hedgehog (Shh) are overexpressed in various cancers, including HNSCC, and have recently been proposed as possible therapeutic targets for HNSCC. Circulating Tumor Cell (CTC) is a novel concept used for the early detection of cancers, and studies have suggested that a higher CTC count is associated with the aggressiveness of HNSCC and poor survival rates. Therefore, we aimed to establish molecular markers for the early diagnosis of HNSCC considering Shh/Nrf2 overexpression in the background. In addition, the relation between Shh/Nrf2 and CTCs is still unexplored in HNSCC patients.</p><p><strong>Methods: </strong>In the present study, we selected a cohort of 151 HNSCC patients and categorized them as CTC positive or negative based on the presence or absence of CTCs in their peripheral blood. Data on demographic and clinicopathological features with the survival of the patients were analyzed to select the patient cohort to study Shh/Nrf2 expression. Shh and Nrf2 expression was measured by qRT-PCR.</p><p><strong>Results: </strong>Considering significant demographic [smoking, betel leaf (p-value < 0.0001)] and clinicopathological risk factors [RBC count (p < 0.05), Platelet count (p < 0.05), Neutrophil count (p < 0.005), MCV (p < 0.0001), NLR (p < 0.05), MLR (p < 0.05)], patients who tested positive for CTC also exhibited significant overexpression of Shh/Nrf2 in both blood and tissue compared to CTC-negative patients. A strong association exists between CTCs and tumor grade. Following chemotherapy (a combination of Cisplatin, 5FU, and Paclitaxel), the frequency of CTCs was significantly decreased in patients with HNSCC who had tested positive for CTCs. The Kaplan-Meier plot illustrated that a higher number of CTCs is associated with poorer overall survival (OS) in patients with HNSCC.</p><p><strong>Conclusions: </strong>Detecting CTCs, and higher expression of Shh and Nrf2 in HNSCC patients' blood, can be a promising tool for diagnosing and prognosticating HNSCC.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10858504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139711455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prioritization of Trypanosoma brucei editosome protein interactions interfaces at residue resolution through proteome-scale network analysis.","authors":"Naghmeh Poorinmohammad, Reza Salavati","doi":"10.1186/s12860-024-00499-4","DOIUrl":"10.1186/s12860-024-00499-4","url":null,"abstract":"<p><strong>Background: </strong>Trypanosoma brucei is the causative agent for trypanosomiasis in humans and livestock, which presents a growing challenge due to drug resistance. While identifying novel drug targets is vital, the process is delayed due to a lack of functional information on many of the pathogen's proteins. Accordingly, this paper presents a computational framework for prioritizing drug targets within the editosome, a vital molecular machinery responsible for mitochondrial RNA processing in T. brucei. Importantly, this framework may eliminate the need for prior gene or protein characterization, potentially accelerating drug discovery efforts.</p><p><strong>Results: </strong>By integrating protein-protein interaction (PPI) network analysis, PPI structural modeling, and residue interaction network (RIN) analysis, we quantitatively ranked and identified top hub editosome proteins, their key interaction interfaces, and hotspot residues. Our findings were cross-validated and further prioritized by incorporating them into gene set analysis and differential expression analysis of existing quantitative proteomics data across various life stages of T. brucei. In doing so, we highlighted PPIs such as KREL2-KREPA1, RESC2-RESC1, RESC12A-RESC13, and RESC10-RESC6 as top candidates for further investigation. This includes examining their interfaces and hotspot residues, which could guide drug candidate selection and functional studies.</p><p><strong>Conclusion: </strong>RNA editing offers promise for target-based drug discovery, particularly with proteins and interfaces that play central roles in the pathogen's life cycle. This study introduces an integrative drug target identification workflow combining information from the PPI network, PPI 3D structure, and reside-level information of their interface which can be applicable to diverse pathogens. In the case of T. brucei, via this pipeline, the present study suggested potential drug targets with residue-resolution from RNA editing machinery. However, experimental validation is needed to fully realize its potential in advancing urgently needed antiparasitic drug development.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10811811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139566776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sumoylation of SAP130 regulates its interaction with FAF1 as well as its protein stability and transcriptional repressor function.","authors":"Chang-Han Chen, Hung-Wei Lin, Meng-Fang Huang, Chi-Wu Chiang, Kuen-Haur Lee, Nguyen Thanh Phuong, Zong-Yan Cai, Wen-Chang Chang, Ding-Yen Lin","doi":"10.1186/s12860-023-00498-x","DOIUrl":"10.1186/s12860-023-00498-x","url":null,"abstract":"<p><strong>Background: </strong>Fas-associated factor 1 (FAF1) is a multidomain protein that interacts with diverse partners to affect numerous cellular processes. Previously, we discovered two Small Ubiquitin-like Modifier (SUMO)-interacting motifs (SIMs) within FAF1 that are crucial for transcriptional modulation of mineralocorticoid receptor. Recently, we identified Sin3A-associated protein 130 (SAP130), a putative sumoylated protein, as a candidate FAF1 interaction partner by yeast two-hybrid screening. However, it remained unclear whether SAP130 sumoylation might occur and functionally interact with FAF1.</p><p><strong>Results: </strong>In this study, we first show that SAP130 can be modified by SUMO1 at Lys residues 794, 878 and 932 both in vitro and in vivo. Mutation of these three SUMO-accepting Lys residues to Ala had no impact on SAP130 association with Sin3A or its nuclear localization, but the mutations abrogated the association of SAP130 with the FAF1. The mutations also potentiated SAP130 trans-repression activity and attenuated SAP130-mediated promotion of cell growth. Additionally, SUMO1-modified SAP130 was less stable than unmodified SAP130. Transient transfection experiments further revealed that FAF1 mitigated the trans-repression and cell proliferation-promoting functions of SAP130, and promoted SAP130 degradation by enhancing its polyubiquitination in a sumoylation-dependent manner.</p><p><strong>Conclusions: </strong>Together, these results demonstrate that sumoylation of SAP130 regulates its biological functions and that FAF1 plays a crucial role in controlling the SUMO-dependent regulation of transcriptional activity and protein stability of SAP130.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10765799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139085855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Dec1 inhibits alcohol-induced hepatic lipid accumulation and circadian rhythm disorder.","authors":"Fuyuki Sato, Ujjal K Bhawal, Kosuke Oikawa, Yasuteru Muragaki","doi":"10.1186/s12860-023-00497-y","DOIUrl":"10.1186/s12860-023-00497-y","url":null,"abstract":"<p><p>Chronic alcohol exposure increases liver damage such as lipid accumulation and hepatitis, resulting in hepatic cirrhosis. Chronic alcohol intake is known to disturb circadian rhythms in humans and animals. DEC1, a basic helix-loop-helix transcription factor, plays an important role in the circadian rhythm, inflammation, immune responses, and tumor progression. We have previously shown that Dec1 deficiency inhibits stresses such as periodontal inflammation and perivascular fibrosis of the heart. However, the significance of Dec1 deficiency in chronic alcohol consumption remains unclear. In the present study, we investigated whether the biological stress caused by chronic alcohol intake is inhibited in Dec1 knockout mice. We treated control and Dec1 knockout mice for three months by providing free access to 10% alcohol. The Dec1 knockout mice consumed more alcohol than control mice, however, we observed severe hepatic lipid accumulation and circadian rhythm disturbance in control mice. In contrast, Dec1 knockout mice exhibited little effect on these outcomes. We also investigated the expression of peroxisome proliferator-activated receptors (PPARs) and AMP-activated protein kinase (AMPK), which are involved in the regulation of fatty acid metabolism. Immunohistochemical analysis revealed increases of phosphorylation AMPK and PPARa but decreases PPARg in Dec1 knockout mice compared to that in control mice. This indicates a molecular basis for the inhibition of hepatic lipid accumulation in alcohol-treated Dec1 knockout mice. These results suggest a novel function of Dec1 in alcohol-induced hepatic lipid accumulation and circadian rhythm disorders.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10763066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139080485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between plasma L-carnitine levels and mitochondrial DNA copy number","authors":"Mingyue Li, Keming Yang, Immaculata De Vivo, A. Heather Eliassen, Abrar A. Qureshi, Hongmei Nan, Jiali Han","doi":"10.1186/s12860-023-00496-z","DOIUrl":"https://doi.org/10.1186/s12860-023-00496-z","url":null,"abstract":"Mitochondria are key cytoplasmic organelles in eukaryotic cells that generate adenosine triphosphate (ATP) through the electron transport chain and oxidative phosphorylation. Mitochondrial DNA (mtDNA) copy number (mtDNAcn) is considered a biomarker for both mitochondrial quantity and function as well as cellular oxidative stress level. Previous epidemiologic findings revealed that weight gain, higher body mass index (BMI), smoking, and high insulinemic potential of lifestyle were associated with lower leukocyte mtDNAcn. Carnitines are a group of compounds that play a critical role in energy production. We quantified the associations of plasma L-carnitine levels with leukocyte mtDNAcn. We then examined the association between mtDNAcn and L-carnitine (HMDB0000062) in 538 U.S. men without cancers, diabetes, or cardiovascular disease at blood collection from the Health Professionals Follow-Up Study (HPFS). We found a significant inverse association between L-carnitine and mtDNAcn (ρ = −0.1, P = 0.02). This implies that the carnitine metabolic pathway may be associated with mitochondrial function and oxidative stress.","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2023-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138566207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Emi1 gene silencing on the proliferation and invasion of human breast cancer cells.","authors":"Ying Kuang, Shengwen Huang, Shifan Tang, Zhaozhen Zhuo, Keyan Linghu","doi":"10.1186/s12860-023-00494-1","DOIUrl":"10.1186/s12860-023-00494-1","url":null,"abstract":"<p><p>Breast cancer is the most common malignant tumour in women. The early silk-splitting inhibitor protein 1 Emi1 is responsible for mediating ubiquitin protein degradation. The present study investigated the effects of the decreased expression of the Emil gene on the proliferation and invasion of breast cancer cells. The interference efficiency of small interfering ribonucleic acid (siRNA) was quantitatively verified using fluorescence real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting, and the effect of Emi1 gene silencing on cell vitality and invasion was determined using MTT and Transwell assays, respectively. The expression of the proliferation genes programmed cell death receptor 4 (PDCD-4), fatty acid synthase ligand (FasL), PTEN and RhoB, along with the invasive genes Maspin, TIMP3 and RECK, was measured using fluorescence RT-qPCR. In breast cancer cells, siRNA successfully reduced the expression of the Emi1 gene, and the expression level of the cell proliferation genes PDCD-4, FasL, PTEN and RhoB, along with invasive genes Maspin, TIMP3 and RECK, decreased significantly (P < 0.05). Furthermore, Emi1 gene silencing reduced the proliferation and invasion abilities of MDA-MB-231 and SUM149PT cells by reducing the expression of proliferative and invasive genes.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10690968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138469895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNFα induces Caspase-3 activity in hematopoietic progenitor cells CD34+, CD33+, and CD41 + of myelodysplastic syndromes.","authors":"Anggraini Iriani, Andhika Rachman, Rahayuningsih D Setiabudy, Siti B Kresno, Aru W Sudoyo, Mansyur Arief, Alida R Harahap, Marsya Kaila Fatina","doi":"10.1186/s12860-023-00495-0","DOIUrl":"10.1186/s12860-023-00495-0","url":null,"abstract":"<p><strong>Background: </strong>Cytopenia is the primary feature of Myelodysplastic Syndrome, even in the presence of hypercellular bone marrow. TNFα is recognized as both a proinflammatory, and proapoptotic cytokine with a well established role in promoting apoptosis in MDS. Therefore, TNFα has the potential to be a valuable biomarker for predicting the progression of cytopenia in MDS. This study aims to establish the role of TNFα exposure in triggering apoptosis through caspase-3 activity in CD34+, CD33+, and CD41 + cells in MDS.</p><p><strong>Methods: </strong>This study is an in vitro comparative experimental research. Bone marrow mononuclear cells were isolated as the source of hematopoietic progenitor cells. Subsequently, CD34+, CD33+, and CD41 + cells were exposed to rhTNFα, and the caspase-3 activity was measured using flowcytometry.</p><p><strong>Results: </strong>In MDS CD33 + and CD41 + caspase-3 activity of rhTNFα exposed cells was significantly higher than without exposed cells. The opposite result was found in CD34 + cells, where the caspase-3 activity without rhTNFα exposed cells was significantly higher than rhTNFα exposed cells.</p><p><strong>Conclusion: </strong>rhTNFα exposure led to an elevation in caspase-3 activity in MDS progenitor cells, especially in those that had differentiated into myeloid cell CD33 + and megakaryocyte cell CD41+, as opposed to the early progenitor cells CD34+.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10662645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138290314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From network analysis to experimental validation: identification of regulators of non-muscle myosin II contractility using the folded-gastrulation signaling pathway.","authors":"Andy Zhao, Sophia Varady, Madelyn O'Kelley-Bangsberg, Vicki Deng, Amy Platenkamp, Petra Wijngaard, Miriam Bern, Wyatt Gormley, Elaine Kushkowski, Kat Thompson, Logan Tibbetts, A Tamar Conner, David Noeckel, Aidan Teran, Anna Ritz, Derek A Applewhite","doi":"10.1186/s12860-023-00492-3","DOIUrl":"10.1186/s12860-023-00492-3","url":null,"abstract":"<p><p>The morphogenetic process of apical constriction, which relies on non-muscle myosin II (NMII) generated constriction of apical domains of epithelial cells, is key to the development of complex cellular patterns. Apical constriction occurs in almost all multicellular organisms, but one of the most well-characterized systems is the Folded-gastrulation (Fog)-induced apical constriction that occurs in Drosophila. The binding of Fog to its cognizant receptors Mist/Smog results in a signaling cascade that leads to the activation of NMII-generated contractility. Despite our knowledge of key molecular players involved in Fog signaling, we sought to explore whether other proteins have an undiscovered role in its regulation. We developed a computational method to predict unidentified candidate NMII regulators using a network of pairwise protein-protein interactions called an interactome. We first constructed a Drosophila interactome of over 500,000 protein-protein interactions from several databases that curate high-throughput experiments. Next, we implemented several graph-based algorithms that predicted 14 proteins potentially involved in Fog signaling. To test these candidates, we used RNAi depletion in combination with a cellular contractility assay in Drosophila S2R + cells, which respond to Fog by contracting in a stereotypical manner. Of the candidates we screened using this assay, two proteins, the serine/threonine phosphatase Flapwing and the putative guanylate kinase CG11811 were demonstrated to inhibit cellular contractility when depleted, suggestive of their roles as novel regulators of the Fog pathway.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10568788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41191061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simple, low-cost, and well-performing method, the outgrowth technique, for the isolation of cells from nasal polyps.","authors":"Jonghui Kim, Karla Hegener, Claudia Hagedorn, Daniel Weidinger, Kashin Jamal Jameel, Inga Marte Charlott Seuthe, Sabine Eichhorn, Florian Kreppel, Jonas Jae-Hyun Park, Jürgen Knobloch","doi":"10.1186/s12860-023-00493-2","DOIUrl":"10.1186/s12860-023-00493-2","url":null,"abstract":"<p><strong>Background: </strong>Epithelial cells are an important part of the pathomechanism in chronic rhinosinusitis with nasal polyps. It is therefore essential to establish a robust method for the isolation and culture of epithelial cells from nasal polyps to enable further research. In this study, the feasibility of the outgrowth technique for the isolation of the epithelial cells from the nasal polyps was evaluated.</p><p><strong>Results: </strong>Using the outgrowth technique, epithelial cells could be isolated from all tissue samples. Isolated epithelial cells showed a proliferation rate of approximately 7- to 23-fold every 6 days up to the 3rd passage. Over 97% of isolated cells were shown to be cytokeratin- and p63-positive, and over 86% of them were Ki-67-positive in flow cytometry. Interleukin-33 and periostin were detectable in the supernatant.</p><p><strong>Conclusions: </strong>We introduce a simple, low-cost, and well-performing method for isolating epithelial cells from nasal polyps with the outgrowth technique.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10566096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41191062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive brain tissue metabolomics and biological network technology to decipher the mechanism of hydrogen-rich water on Radiation-induced cognitive impairment in rats.","authors":"Xiaoming Liu, Mengya Liu, Huan Liu, Hui Yuan, Yong Wang, Xiaoman Chen, Jianguo Li, Xiujun Qin","doi":"10.1186/s12860-023-00491-4","DOIUrl":"10.1186/s12860-023-00491-4","url":null,"abstract":"<p><strong>Background: </strong>Hydrogen-rich water (HRW) has been shown to prevent cognitive impairment caused by ionizing radiation. This study aimed to investigate the pharmacological effects and mechanisms of HRW on ionizing radiation by coupling the brain metabolomics and biological target network methods.</p><p><strong>Methods and results: </strong>HRW significantly improves the cognitive impairment in rats exposed to ionizing radiation. Based on metabolomics and biological network results, we identified 54 differential metabolites and 93 target genes. The KEGG pathway indicates that glutathione metabolism, ascorbic acid and aldehyde acid metabolism, pentose and glucuronic acid interconversion, and glycerophospholipid metabolism play important roles in ionizing radiation therapy.</p><p><strong>Conclusion: </strong>Our study has systematically elucidated the molecular mechanism of HRW against ionizing radiation, which can be mediated by modulating targets, pathways and metabolite levels. This provides a new perspective for identifying the underlying pharmacological mechanism of HRW.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10523633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41105908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}